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Descriptions

Maize defective kernel (dek) mutants identify genes necessary for the
successful passage of embryos through the embryogenic and maturation
phases of embryo development. The goal of this thesis was to characterize the
developmental potential of three dek mutants that appeared to be
morphologically blocked prior to the maturation phase of embryogenesis.
Descriptive and experimental studies of the mutants and their wild-type
counterparts were used to compare their morphological and physiological
progression through seed development. Parameters of growth,
morphogenesis, maturation and germination were measured throughout their
ontogeny. Two mutants, cp*-1311C and cp*-1399A, slowly progress to
morphological stages 2 and 3, respectively. Growth and maturation processes
remain in synchrony with morphology, as indicated by their size, germination
behavior and level of storage reserve accumulation. Not every facet of
development is retarded. Both dehydration of the seed and the accumulation of
desiccation proteins, maize Lea group 3 (MLG3) and Lea group 2 dehydrin
(DHN), are more globally regulated, since their accumulation is precocious with
respect to embryo morphology. This suggests that some aspects of the
embryonic program are mediated by maternal factors. Genetic and
developmental characterization of a third mutant, dks8, indicates that it defines
a pattern gene that functions to specify the initiation or maintenance of the
embryonic shoot. The dks8 mutant is variable in phenotype; mutants with
partial and abnormal shoot development are sometimes found on ears
segregating for shootless dks8 embryos. dks8 is not allelic to other shootless
dek mutants. The dks8 mutation was isolated from an active Mutator
transposon stock. RFLP analyses for cosegregation of various Robertson's
Mutator transposable elements with the dks8 allele demonstrate that a Mu8
element and dks8 are closely linked. The dks8 allele is under-represented on
segregating ears, which may reflect either epigenetic suppression of the mutant
phenotype or a bias against the mutant allele in the formation of the female
gametophyte.